@article{SCI15269,
author = {Rozenn Quarck and Fréderic Perros},
title = {Rescuing BMPR2-driven endothelial dysfunction in PAH: a novel treatment strategy for the future?},
journal = {Stem Cell Investigation},
volume = {4},
number = {6},
year = {2017},
keywords = {},
abstract = {Pulmonary arterial hypertension (PAH) may be idiopathic and corresponds to sporadic disease without any familial history or identified risk factors, or heritable when it occurs in the hereditary context; germline mutations in the bone morphogenetic protein receptor type 2 (BMPR2) gene, are detected in 70% of heritable PAH cases (1). Even in sporadic cases, PAH is associated with impaired BMPRII signalling, occurring through small mothers against decapentaplegic (SMAD) proteins (2).},
issn = {2313-0792}, url = {https://sci.amegroups.org/article/view/15269}
}